Therapeutic implications of recent findings in feline renal insufficiency (Proceedings) - Veterinary Healthcare
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Therapeutic implications of recent findings in feline renal insufficiency (Proceedings)


CVC IN KANSAS CITY PROCEEDINGS


The term chronic renal insufficiency (CRI) is preferable to chronic renal failure (CRF), permitting us to view the condition as a progressive one, rather than imminently terminal and encourage our clients to treat their companions. Cats often live for many years with decreased urine specific gravity, elevations in BUN and creatinine after initial detection depending on the stage and cause of the disease. Some causes of renal insufficiency are more rapidly progressive or fatal than others; others are benign. Causes of chronic renal insufficiency include, in decreasing order of occurrence, chronic (tubulo-) interstitial nephritis (CIN), pyelonephritis, renal neoplasia, FIP, amyloidosis, congenital abnormalities, polycystic kidney disease, perinephric pseudocysts, nephrolithiasis, hydronephrosis, glomerulonephritis, potassium losing nephropathy, and polyarteritis nodosa. CIN and pyelonephritis are most common.

Causes of acute renal failure are renal ischemia and nephrotoxicosis. The former may have pre-renal, renal or post-renal causes. Reduced renal perfusion leads to prerenal azotemia but may progress to failure if ischemia of significant severity is present for long enough. Anesthesia, hypotension, hypovolemia are causes. By monitoring blood pressure we can intervene with fluids and oxygen/oxygen carrying fluids generally preventing progression from pre-renal to renal failure. Severe ischemic injury in the cat is caused by thromboembolism of the renal arteries due to cardiomyopathy, extensive renal infarction and subsequent intra-renal acute renal failure. Renal toxins include ethylene glycol, Easter lilies, grapes and raisins, film processing chemicals, heavy metals, aminoglycoside antibiotics (by any route), amphotericin B, and doxorubricin (uncommon in cats). Uremia is defined as the "constellation of clinical signs" seen with markedly decreased glomerular filtration rates (GFR). Uremia is usually not seen until BUN > 80 mg/dl (28 mmol/L) and serum creatinine > 4.0 mg/dl (354 μmol/L) AFTER rehydration. Signs include lethargy, depression, anorexia, and vomiting.

Renal physiology: Functions of the kidneys

1) remove toxic metabolites from the body

2) reabsorb/conserve salts, glucose, proteins, electrolytes and water

3) regulate blood pressure

4) regulate acid/base balance

5) endocrine functions: produce renin, erythropoeitin, prostaglandins and convert precursor to active form of Vitamin D3/ dihydroxycholecalciferol

There is no single test measure renal function. The ability of the kidney to reabsorb water from the tubules is reflected by urine specific gravity (usg). Proteins must be conserved and not lost, thus testing for proteinuria is another way to look at renal function. Removal of toxic metabolites is the renal function we usually focus on because blood urea nitrogen (BUN) and creatinine (Cr) are on chemistry panels. The ability to concentrate urine (tubular, usg) is lost when 2/3 of nephrons are lost. Later, when approximately of nephrons are lost, impairment of glomerular function is evident by increasing BUN and SC.

Hypokalemia is very common in cats with renal insufficiency. The kidney is the main site in the body for potassium (K) homeostasis. Approximately 80% of K is reabsorbed in the proximal tubules and the loop of Henle. Three major factors affect the movement of potassium: 1) the magnitude of the concentration gradient, which is mediated by the Na-K-ATPase pump, 2) the rate of tubular flow, and 3) the electrical transmembrane potential difference across the luminal membrane of the tubular cell. Final adjustments to the net reabsorption or excretion of K occur in the collecting ducts and are mediated by aldosterone, Na, K concentration, acidosis and diuretics. Animals making a lot of urine (PU/PD) have a fast rate of tubular flow. Predisposing them to hypokalemia.

As GFR decreases in renal insufficiency, phosphorus is retained in the blood, causing transient hyperphosphatemia. Initially, remaining nephrons compensate by increasing their excretion levels; this action is mediated by parathyroid hormone (PTH). Eventually, as chronic renal insufficiency progresses and glomerular filtration rate (GFR) decreases to less than 20% of normal, this compensatory mechanism fails and persistent hyperphosphatemia results and renal secondary hyperparathyroidism ensues.


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